Fives-Taylor P M, Meyer D H, Mintz K P, Brissette C
Department of Microbiology & Molecular Genetics, University of Vermont, Burlington, USA.
Periodontol 2000. 1999 Jun;20:136-67. doi: 10.1111/j.1600-0757.1999.tb00161.x.
A. actinomycetemcomitans has clearly adapted well to its environs; its armamentarium of virulence factors (Table 2) ensures its survival in the oral cavity and enables it to promote disease. Factors that promote A. actinomycetemcomitans colonization and persistence in the oral cavity include adhesins, bacteriocins, invasins and antibiotic resistance. It can interact with and adhere to all components of the oral cavity (the tooth surface, other oral bacteria, epithelial cells or the extracellular matrix). The adherence is mediated by a number of distinct adhesins that are elements of the cell surface (outer membrane proteins, vesicles, fimbriae or amorphous material). A. actinomycetemcomitans enhances its chance of colonization by producing actinobacillin, an antibiotic that is active against both streptococci and Actinomyces, primary colonizers of the tooth surface. The fact that A. actinomycetemcomitans resistance to tetracyclines, a drug often used in the treatment of periodontal disease, is on the rise is an added weapon. Periodontal pathogens or their pathogenic products must be able to pass through the epithelial cell barrier in order to reach and cause destruction to underlying tissues (the gingiva, cementum, periodontal ligament and alveolar bone). A. actinomycetemcomitans is able to elicit its own uptake into epithelial cells and its spread to adjacent cells by usurping normal epithelial cell function. A. actinomycetemcomitans may utilize these remarkable mechanisms for host cell infection and migration to deeper tissues. A. actinomycetemcomitans also orchestrates its own survival by elaborating factors that interfere with the host's defense system (such as factors that kill phagocytes and impair lymphocyte activity, inhibit phagocytosis and phagocyte chemotaxis or interfere with antibody production). Once the organisms are firmly established in the gingiva, the host responds to the bacterial onslaught, especially to the bacterial lipopolysaccharide, by a marked and continual inflammatory response, which results in the destruction of the periodontal tissues. A. actinomycetemcomitans has at least three individual factors that cause bone resorption (lipopolysaccharide, proteolysis-sensitive factor and GroEL), as well as a number of activities (collagenase, fibroblast cytotoxin, etc.) that elicit detrimental effects on connective tissue and the extracellular matrix. It is of considerable interest to know that A. actinomycetemcomitans possesses so many virulence factors but unfortunate that only a few have been extensively studied. If we hope to understand and eradicate this pathogen, it is critical that in-depth investigations into the biochemistry, genetic expression, regulation and mechanisms of action of these factors be initiated.
伴放线放线杆菌显然已很好地适应了其生存环境；其一系列毒力因子（表2）确保了它在口腔中的存活，并使其能够引发疾病。促进伴放线放线杆菌在口腔中定植和持续存在的因素包括黏附素、细菌素、侵袭素和抗生素耐药性。它能够与口腔的所有组成部分（牙齿表面、其他口腔细菌、上皮细胞或细胞外基质）相互作用并黏附。这种黏附由许多不同的黏附素介导，这些黏附素是细胞表面的成分（外膜蛋白、囊泡、菌毛或无定形物质）。伴放线放线杆菌通过产生放线杆菌素提高其定植几率，放线杆菌素是一种对链球菌和放线菌均有活性的抗生素，而链球菌和放线菌是牙齿表面的主要定植菌。伴放线放线杆菌对常用于治疗牙周病的四环素的耐药性正在上升，这是它的又一“武器”。牙周病原体或其致病产物必须能够穿过上皮细胞屏障，才能到达并破坏下方组织（牙龈、牙骨质、牙周膜和牙槽骨）。伴放线放线杆菌能够通过篡夺正常上皮细胞功能使自身被上皮细胞摄取并扩散至相邻细胞。伴放线放线杆菌可能利用这些非凡机制感染宿主细胞并迁移至更深层组织。伴放线放线杆菌还通过分泌干扰宿主防御系统的因子（如杀死吞噬细胞和损害淋巴细胞活性、抑制吞噬作用和吞噬细胞趋化性或干扰抗体产生的因子）来精心策划自身的生存。一旦这些微生物在牙龈中牢固定植，宿主就会对细菌的攻击，尤其是细菌脂多糖，做出明显且持续的炎症反应，这会导致牙周组织的破坏。伴放线放线杆菌至少有三种导致骨吸收的独立因子（脂多糖、蛋白水解敏感因子和热休克蛋白GroEL），以及许多对结缔组织和细胞外基质产生有害影响的活性物质（胶原酶、成纤维细胞细胞毒素等）。令人感兴趣的是，伴放线放线杆菌拥有如此多的毒力因子，但遗憾的是只有少数因子得到了广泛研究。如果我们希望了解并根除这种病原体，关键是要对这些因子的生物化学、基因表达、调控及作用机制展开深入研究。
